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Atrial Natriuretic Peptide Extends Lung Preservation Attenuating Ischemia-Reperfusion Lung Injury Through Phospholipase A2 Inhibition
Yury A. Bellido Reyes, Prudencio Díaz-Agero, Joaquin García S. Girón; Thoracic Surgery, La Paz Hospital, Madrid, Spain
READER COMMENTS
Objective: Phospholipase A2 (PLA2), a key enzyme in the regulation of the arachidonic acid metabolism, is potentially involved in the physiopathology of ischemia-reperfusion (IR) injury. In the present study, we hypothesized that supplementation of low potassium dextram (LPD) solution with atrial natriuretic peptide (ANP) extends lung preservation attenuating IR lung injury through inhibition of the PLA2 cascade.
Methods: To test the hypothesis, we examined the effects of ANP in an isolated rat lung model. Three groups were defined (n = 6, each): in the vehicle group, lungs were perfused for 2 hours without an ischemic period. In two ischemic groups, lungs were flushed with low potassium dextram solution (LPD group) or LPD containing 10 nM of ANP (LPD+ANP group), cold-stored 18 hours, and reperfused for 2 hours.
Results: Isquemia-reperfusion reduced PO2 from 615.7 ± 28.5 to 452.1 ± 28.2 mmHg (p<0.001), at the end of reperfusion in the LPD group. Compared to the vehicle group the pulmonary artery pressure, airway pressure, wet-to-dry ratio, proteins in BAL, and myeloperoxidase activity increased significantly in the LPD group, (p<0.05) respectively. In addition, IR increased significantly cytosolic and soluble phospholipase A2 activity together with thromboxane and leukotriene formation in the LPD group compare to vehicle; while supplementation of the preservation solution with ANP decreased all these maintaining the PO2 at a level similar to the vehicle group throughout reperfusion and decresed significantly the alveolar-capillary leakage, edema formation and neutrophil extravasation.
Conclusion: Supplementation of the preservation solution with atrial natriuretic peptide extends the preservation properties of LPD solution attenuating IR injury through inhibition of the phospholipase A2 cascade.

Edema formation, neutrophil extravasation, and phospholipase A2 metabolism after ischemia-reperfusion
Wet-to-dry ratio Proteins BALFMPO activitycPLA2 activitysPLA2 activityThromboxan A2Leukotriene B4
mg/mLOD/mg/minnmol/mg/minnmol/mg/min pg/mL pg/mL
Vehicle group6.22 ± 0.37 §0.17 ± 0.07 §0.44 ± 0.06 §1.15 ± 0.14 §171.8 ± 38.2 §203.3 ± 70.9 §132.4 ± 68.8 §
LPD group10.97 ± 1.401.01 ± 0.151.21 ± 0.151.63 ± 0.18350.3 ± 84.3826.1 ± 213.0392.3 ± 77.3
LPD+ANP group6.62 ± 1.24 §0.38 ± 0.09 ¶0.62 ± 0.05 §1.12 ± 0.21 § 239.3 ± 62.0 §495.5 ± 97.9 §,¶253.6 ± 63.0 §,¶

Values are mean ± SEM (n = 6, per group). BALF, bronchoalveolar lavage fluid; MPO, myeloperoxidase; cPLA2, cytosolic phospholipase A2; sPLA2, soluble phospholipase A2. (§) p<0.01 vs LPD group, (¶) p<0.05 vs vehicle group.
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